Articles: cations.
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Historical Article
Vesalius and His Manikin: An Enduring Influence on Modern Anatomic Teaching.
Anatomic teaching has long informed surgical knowledge, experience, and skills. One tool for teaching that emerged during the Renaissance was the fugitive anatomic sheet, which used flap layers to reveal different levels of anatomy. In 1538, Vogtherr introduced the first fugitive sheets, which included illustrations of male and female figures with a torso paper flap that, when lifted, revealed the internal organs in a cartoonish style. ⋯ Vesalius's groundbreaking discoveries, his use of the most advanced printing techniques, and his innovative teaching style are fundamental aspects of the legacy of medical education. This article shows these remarkable fugitive anatomic sheets from the original publications of Fabrica and Epitome together for the first time. It explores the innovative concepts and applications of Vesalius's unique printings.
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Chronic pain is common among children and adolescents; however, the diagnoses in the newly developed 11th revision of the International Classification of Diseases (ICD-11) chronic pain chapter are based on adult criteria, overlooking pediatric neurodevelopmental differences. The chronic pain diagnoses have demonstrated good clinical applicability in adults, but to date, no field study has examined these diagnoses to the most specific diagnostic level in a pediatric sample. The current study aimed to explore pediatric representation within the ICD-11, with focus on chronic primary pain. ⋯ The latter also exhibited the lowest agreement between HCPs and algorithm. The current study underscores the need for evidence-based improvements to the ICD-11 diagnostic criteria in pediatrics. Developing pediatric coding notes could improve the visibility of patients internationally and improve the likelihood of receiving reimbursement for necessary treatments through accurate coding.
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Sepsis-associated acute kidney injury (SAKI), a common complication in intensive care units (ICUs), is linked to high morbidity and mortality. Sirtuin 2 (SIRT2), an NAD + -dependent deacetylase, has been shown to have distinct effects on autophagy regulation compared to other sirtuins, but its role in SAKI remains unclear. This study explored the potential of SIRT2 as a therapeutic target for SAKI. ⋯ Consistent with in vivo findings, SIRT2 gene silencing promoted autophagy in LPS-treated HK-2 cells, whereas SIRT2 overexpression inhibited it. Mechanistically, SIRT2 inhibition increased FOXO1 acetylation, inducing its nuclear-to-cytoplasmic translocation, which promoted kidney autophagy and alleviated SAKI. Our study suggests SIRT2 as a potential target for SAKI therapy.
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Na v 1.9 is of interest to the pain community for a number of reasons, including the human mutations in the gene encoding Na v 1.9, SCN11a , that are associated with both pain and loss of pain phenotypes. However, because much of what we know about the biophysical properties of Na v 1.9 has been learned through the study of rodent sensory neurons, and there is only 76% identity between human and rodent homologs of SCN11a , there is reason to suggest that there may be differences in the biophysical properties of the channels in human and rodent sensory neurons, and consequently, the contribution of these channels to the control of sensory neuron excitability, if not pain. Thus, the purpose of this study was to characterize Na v 1.9 currents in human sensory neurons and compare the properties of these currents with those in rat sensory neurons recorded under identical conditions. ⋯ However, we noted a number of potentially important differences between the currents in human and rat sensory neurons including a lower threshold for activation, higher threshold for inactivation, slower deactivation, and faster recovery from slow inactivation. Human Na v 1.9 was inhibited by inflammatory mediators, whereas rat Na v 1.9 was potentiated. Our results may have implications for the role of Na v 1.9 in sensory, if not nociceptive signaling.
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Liver ischemia reperfusion (IR) injury significantly impacts clinical outcomes by increasing the risk of hepatic dysfunction after liver surgery. Fatty livers are more susceptible to IR stress. Recent studies have demonstrated that S100A9 plays a crucial role in both IR injury and the progression of liver steatosis. ⋯ Intriguingly, S100A9 facilitated ATF4 nuclear translocation and enhanced NEK7/NLRP3 inflammasome activation in macrophages. In conclusion, our study identified S100A9 as a key regulator responsible for macrophage NLRP3 inflammasome activation and subsequent inflammatory injury in fatty liver IR process. Targeting TLR2/ATF4 signaling may offer a novel therapeutic strategy for mitigating S100A9-mediated liver injury.